Saturday, November 19, 2016

In the previous two blogs I have shown that blood lead is
not a simple measure of exposure. In an given setting of environmental exposure
from air pollution, water pollution or ingestion, blood lead levels are
influenced by vitamin deficiencies, magnesium, potassium, zinc, and iron
deficiency. These deficiencies
influence the uptake of cadmium as well as lead.

In comparing 16
metals, cadmium was the most toxic and about 200 times more toxic than lead in
an experiment where metals were given to
a rodent and the toxic effect was lowering body temperature and negatively influencing mitochondrial function
as evidenced by decreasing consumption of oxygen (Gordon 1990). Cadmium is a ubiquitous pollutant. It is
present in all cells. In a setting of
stress, free cadmium appears to be released from the lining of
blood vessels and or the choroid plexus and triggers an acute stress reaction. Cadmium influences bone metabolism resulting
in activation of osteoclasts (Sughis
2011). This is an effect blocked by
zinc (Baljit S 1995). Resorption of bone releases lead which is stored in bone
into blood, elevating blood lead levels
from a toxic effect of cadmium.

Children who live in poverty
with dietary deficiencies,
emotional stress, and often co-exposure to cadmium in environmental tobacco
smoke or other chemicals which are synergistic with cadmium, will have blood lead levels that are higher
than children without these factors.
Blood lead elevations are a useful marker of children in need of intervention. The lead programs set up to help these children
need to focus on the dietary deficiencies and cadmium exposures. The lack of correlation with blood cadmium is
not evidence that cadmium is not involved. It disappears readily into the blood
vessel lining so that blood cadmium levels do not necessarily correlate with
exposure or toxic effect.

In the 1994-2004 NHANES study, children aged 6 to 15 in the highest quartile of urine cadmium had a three fold risk of
placement in special education placement (Ciesielski et al 2012). Urine cadmium, however, is not a simple
measure of exposure, either. This study
is consistent with my finding that children exposed to cadmium and in the
highest quartile of hair cadmium had the lowest achievement. Although there was
no linear correlation with hair cadmium and achievement, there was a
correlation with hair lead even though there was no increased lead exposure in
the affected children.

In a Japanese study,
the urine cadmium of women with breast cancer who knew they had breast cancer was much higher
than the urine cadmium of women who were screened for breast cancer and did not
know they had the disease (Nagata C 2013).
In an American study (McElroy et
al 2005) women in the highest quartile for cadmium had twice the risk of breast cancer. In the most recent American study ( Adams et al 2016) there was no correlation between quartiles of urinary cadmium and breast
cancer.

Urine cadmium in men in NHANES III, however, was associated with
all cause mortality, cancer mortality, and specifically prostate cancer
mortality ( (Cheung M 2014). Urine
cadmium in women was higher but not associated with any specific disease. Urine cadmium in the same NHANES III was correlated with impaired glucose tolerance
and diabetes.

Just as with lead, deficiencies
of vitamins and minerals and processed
food that contains bisphenol A can
increase the uptake and toxicity of cadmium.
Children and adults with higher
urine cadmium need the same assessment and treatment as those with small
elevations of blood lead .

Toxicity to cadmium can occur in the absence of any exposure
to lead. Toxicity to lead except in acute ingestions resulting in blood
lead levels over 40 mcg/dL occurs with co-exposure
to cadmium but correlations with blood, hair, and urine cadmium levels are
inconsistent. Neither blood, urine, or hair cadmium is a marker of acute or chronic exposure. It is variable and
strongly influenced by stress which transiently releases it from blood vessels.

The magnitude of this reservoir is evident from a study by
Koizumi in 1994 in Japan. Blood cadmium levels at autopsy were a hundred times
higher than while living. This increase
was seen only for cadmium and not other metals. Blood cadmium levels would undoubtedly be
higher in current smokers and past smokers. Blood cadmium of non smokers at
autopsy would provide useful information regarding environmental exposure
to cadmium, especially cadmium air pollution.

Thursday, November 17, 2016

How
can a toxic effect of cadmium cause a small elevation of blood or hair lead
above the average for that environment?

To
understand the behavior of metals it is necessary to look at their biochemical
behavior. Statistical correlations can
be misleading. It has been known for a long time that zinc and iron
deficiencies were associated with toxic effects of lead. These deficiencies are known to increase the absorption
and toxicity of cadmium. The inhibition
of the enzyme ALAD which is considered particularly characteristic of toxicity to
lead occurs with cadmium. Zinc protects this enzyme from inhibition. Cadmium
is an anti-metabolite of zinc. Zinc protects cells from cadmium toxicity. So
lead toxicity is not just a simple matter of exposure to a toxic metal and a
toxic effect that one can measure with blood lead levels or inhibition of
ALAD.

An excellent article is available regarding the
use of dietary strategies for the treatment of lead and cadmium toxicity.

In
this article the effects of vitamins, minerals, herbs, and probiotics on toxic
effects of lead and cadmium are discussed. In most cases it is clear that a
reduction of blood lead with these strategies also reversed toxic effects of
cadmium.

One could consider that both
lead and cadmium are toxic but that elevation of blood lead is the indicator of
toxicity, not blood cadmium. Certainly
the toxicity is directly associated with deficiencies of vitamins and minerals.
However, one could also consider that lead exposure directly influences the
uptake of cadmium.

Cadmium is very interactive with all nutrient
and toxic metals and also with toxic chemicals. Lead is treated more like
calcium in the body and is stored in bone. Cadmium is stored in the lining of
blood vessels and in the choroid plexus surrounding the brain. It is in the
kidney, liver, ovary, testes, thyroid, and adrenals. With acute stress, like
handling an animal, cadmium is released into the body. Consequently, cadmium effects can occur
without directly adding cadmium to an experimental animal.

Cadmium
causes a stress response in all cells. Lead does so only through increasing the
absorption of cadmium. For instance,
lead in water increases metallothionein production in the liver. Metallothionein is part of the acute stress
response that cadmium produces. Cadmium
activates the promotor of metallothionein
whether cadmium has been added in the
experiment or not. When lead is directly added to liver cells there is no
increase in metallothionein production. Lead in drinking water increases the uptake of
cadmium which promotes the stress response resulting in increased metallothionein
production. It is not just that lead and
cadmium are both toxic. Toxic effects attributed
to lead are caused by cadmium.

It
is this effect of lead ingestion increasing the absorption of cadmium that is
directly related to the small but significant elevations in blood lead levels
and health effects. Cadmium increases resorption
of bone where lead is stored increasing blood lead levels. So the level of lead in blood is not a
measure just of exposure,but exposure plus a toxic effect of cadmium on bone.
Blood cadmium is not a helpful measurement because cadmium is taken up rapidly
into the blood vessels and the various organs.
The levels are highly variable through the day responding to various stresses. Blood hair, and urine cadmium levels are not
just measures of exposure but also of stressed induced releases.

Based on this information alone, it is clear
that cadmium is important. It should be measured accurately in air. New
approaches are needed to detect these volatile ultrafine fumes of cadmium. The US EPA needs to fund research on
effective ways to measure cadmium. Children with elevated blood lead levels
should be evaluated for toxic effects of cadmium. Their urine cotinine should be measured to determine
exposure to environmental tobacco smoke.
Children in tee highest quartile of urine cadmium have a three fold risk
for placement in special education. These children need the dietary strategies
suggested by Q Zhai et al. They need
stress reduction and excellent care both at home and at school. They are not permanently
damaged. It is neglect and indifference that
leads to permanent damage in most instances.

Sandra
M. Pinkham, M.D< Time for A Change>. 11-17-2016 > > > Since
lead was taken out of gasoline in 1980, the public has been told that lead is
the most serious toxic agent. Flint Michigan parents were told that their children
were being permanently damaged by exposure to lead in water. The public
has been old that removing lead from gasoline which lowered blood lead levels
dramatically has made the air cleaner. What is wrong with this message? >In the last 30 years I have made an
extensive search of the world literature on lead and cadmium and
other toxic substances known to have an adverse effect on health. This was
triggered by a finding in a hair analysis study that I did on children in 1986.
The children in my study with the highest levels of lead and cadmium in their
hair had the lowest scores on achievement. This was statistically significant
for lead but not cadmium. All the children were exposed to cadmium from a
large waste incineration plant in operation for 2 years, a very significant
source of cadmium pollution and other chemicals that act in synergy with
cadmium. Only 2 of the 60 were exposed to passive smoke, another very
significant source of cadmium air pollution exposure in humans. The
children with the higher levels of lead and cadmium were experiencing stress
from having learning problems. The hair lead levels were associated with very
low levels of blood lead. The children had minimal exposure to lead.
Although the cadmium levels were elevated in the children with learning
problems, the high variability in hair cadmium compared to hair lead resulted
in an insignificant statistical correlation. > >From my literature search, I discovered that it
is the statistical correlation of small
elevations of blood leads at any level along the line from a blood lead of 20
ug/dL to zero that is the main proof that lead is so toxic. In studies where
lead is given for long periods of time to show adverse effects in experimental animals,
there was no attempt to see what happens to other metals, especially cadmium in
most studies. In the few where that was studied researchers showed that ingestion
of lead in water increased cadmium uptake into the brain. Just the fact that when blood lead levels
averaged 15 the toxic children had blood lead levels of 20 and when the average
was 5 the toxic children had 10 and now when the average blood lead level is
less than one a blood lead level of 5 is considered toxic should make one
suspicious that lead exposure may not be the cause of the linear correlation. .
Clearly all the children in the 1960’s
and 70s were not being poisoned by lead.

An alternate explanation which makes more
sense is that blood lead is not just an indicator of exposure. Small increases
over a background level is actually an indicator of a toxic effect that is
increasing the presence of lead ions in blood. My next blog will explain the
biochemical basis for this effect.

About Me

As a medical practioner for over 20 years I felt the need to increase healthy living through reducing stress, improving diet and lifestyle. I am passionate about getting people to know about heavy metal toxicity and the damage it does to our health and our environment.